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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 292 (2000), S. 562-567 
    ISSN: 1432-069X
    Keywords: Keywords Vitamin B6 ; UVA ; Phototoxicity ; ESR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously reported that pyridoxine shows UVA-induced cytotoxicity. Four other vitamin B6 compounds (pyridoxal, pyridoxamine, pyridoxal phosphate, and pyridoxamine phosphate) are metabolically more important in vivo than pyridoxine. These compounds were examined for UVA phototoxicity to cultured human fibroblasts. The cytotoxicity was measured by post-UVA irradiation colony-forming ability. All the B6 compounds except pyridoxal phosphate showed cytotoxicity. Pyridoxamine phosphate, which is the most important form of vitamin B6 in vivo, had the strongest cytotoxic effect. To examine the involvement of reactive oxygen species in the phototoxicity, we performed an electron spin resonance study using the spin trapping agent, 5,5-dimethyl-1-pyrroline N-oxide, and diethylenetriaminepentaacetic acid. We failed to detect radicals derived from vitamin B6. The cytotoxic effect remained in UVA-irradiated solutions for at least 30 min after the end of UVA irradiation. Hydrogen peroxide was produced in the solution, but the amount was not enough to cause cytotoxicity. In addition, the cells from xeroderma pigmentosum patients who belong to group A or C showed survival curves similar to those of normal fibroblasts. This suggests that cyclobutane pyrimidine dimers or 6-4 photoproducts of DNA were not involved in this damage. These findings suggest that UVA-induced vitamin B6 cytotoxicity is caused by toxic photoproducts resulting from irradiated vitamin B6.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2277
    Keywords: Key words Biliary epithelial cells ; TGF-β1 rat ; Mixed lymphocyte reaction ; CTL
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Immune response to liver allografts may be different from that to other organ transplants since immunological manipulation easily attenuates immune-response to liver allografts. Numerous studies on the alloantigen-specific immune response have been carried out, however, the precise mechanisms involved in this attenuation are not clear yet. Here we suggest the attenuation of alloantigen-specific immune response by TGF-β1 derived from biliary epithelial cells. The transforming growth factor-β1 (TGF-β1) expression in rat liver was examined immunohistologically. Rat biliary epithelial cells (BEC) were purified from the perfused liver and added to allogeneic mixed lymphocyte reaction (allo-MLR) to assess their attenuating potential on allo-MLR and alloantigen-specific cytotoxic T lymphocyte (allo-CTL) induction. Immunohistological investigation revealed the expression of TGF-β1 in biliary epithelial cells. Both purified biliary epithelial cells and TGF-β1 attenuated allo-MLR and allo-CTL induction in a dose-dependent manner, and anti-TGF-β1 antibody partially relieved this attenuation. This study reveals that biliary epithelial cells, the major target cells of allo-antigen specific immune response, contain TGF-β1 and that they have a capacity to attenuate allo-MLR and allo-CTL induction.
    Type of Medium: Electronic Resource
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